Among patients with chronic renal failure, the nervous system is the "barometer" of general well being. Despite impressive modification of both the duration and "quality" of life by dialysis, renal transplantation and improved medical management, patients with renal failure continue to manifest a variety of neurological disorders. Patients with chronic failure not yet requiring dialytic therapy may have a symptom complex which can include weakness, impaired memory, inability to concentrate, apathy, and lethargy. These symptoms are modified by dialytic therapy, but persist to some degree with frequent addition of impotence, progressive intellectual impairment and dementia. The biochemical basis for any of the aforementioned abnormalities is unclear. The present study is designed to investigate the biochemical basis of uremic encephalopathy. It is proposed to evaluate, in animal models of chronic renal failure, the following: Identification of parathyroid hormone receptors in brain and how they are affected by renal failure; the brain redox state, and brain energy metabolism. The nervous system manifestations of the uremic state are among the most disabling to the patient with chronic renal failure. Elucidation of the pathophysiologic mechanisms of these disorders should lead to more effective therapy. This should in turn lead to both a more productive existence, as well as an improved "quality of life" for these patients.